Autism, a neurodevelopmental disorder diagnosed yearly in 1/500 to 1/1000 children in the United States, is typified by delayed language and abnormal sound sensitivity. While these impairments are pervasive features of, autism, their description is based largely on clinical observations and the etiology is unknown. Progress in understanding the neural bases of language and sound processing abnormalities has been hampered by the highly variable manifestations of impairment coupled with the complexities of the human auditory system. As a result, there is at present no unitary model for or comprehensive description of auditory dysfunction in autism disorder (AD). In this application, we propose experiments that combine a relatively rare neuroimaging technique (Magnetoencephalography (MEG)) with a well-characterized sample in order to accelerate our knowledge of the pathophysiology of AD. MEG is an emergent neuroimaging technique that allows us to non-invasively measure synchronized responses of population of neurons. Importantly, MEG has been demonstrated to be well tolerated by children with AD. Recent evidence for slowed neural conduction times at the auditory brainstem in autistic children combines with our preliminary MEG data showing general prolongation in cortical evoked responses in children with AD to motivate the present investigation. Our overarching hypothesis is that language impairment and sound reactivity in AD children stem from impairments at the sensory level and may have multiple loci in the ascending auditory system. Cumulatively these data combine with observed sensory and language dysfunction in children with AD to raise several core questions. First, what is the association between perceptual acuity and cortical auditory function in children with autism? Aim 1 addresses this question by combining psychophysical experimentation with MEG recording in a within subjects design. Second, what is the correspondence between sensory reactivity observed in AD children and abnormal loudness growth? Next, how does abnormal loudness perception relate to dysfunction in neural mechanisms for decoding intensity cues? Aim 2 addresses this issue with both psychophysical and MEG testing. Finally, what is the correspondence between slowed neural conduction times at peripheral and subcortical auditory sites and those found at the level of auditory cortex? Aim 3 addresses this question using a combination of electrophysiology and MEG recording.